Heart failure (impaired ventricular pump function) is an eventual outcome for diverse cardiovascular disorders and the leading cause of combined morbidity and mortality in the United States and other developed industrial nations. The focus of my lab is to understand the molecular mechanisms that initiate and mediate the pathogenesis of maladaptive cardiac remodeling, such as cardiac hypertrophy and fibrosis. The overall approach consists of using molecular and genetic engineering mouse models by generating constitutive and inducible transgenic mice as well as straight and conditional knockout mice with different cardiomyopathy.